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1000 Titel
  • Dissecting the dynamics of cell death pathways in Hirschsprung’s disease: a comparative analysis of viable and non-viable cells under proinflammatory conditions
1000 Autor/in
  1. Li, Zhongwen |
  2. Hagens, Johanna |
  3. Philippi, Clara |
  4. Schmidt, Hans Christian |
  5. Rohwäder, Lucie |
  6. Schuppert, Pauline |
  7. Pagerols Raluy, Laia |
  8. Trochimiuk, Magdalena |
  9. Reinshagen, Konrad |
  10. Tomuschat, Christian |
1000 Verlag Springer Berlin Heidelberg
1000 Erscheinungsjahr 2024
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2024-11-03
1000 Erschienen in
1000 Quellenangabe
  • 40(1):288
1000 Copyrightjahr
  • 2024
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1007/s00383-024-05862-2 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532316/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • <jats:title>Abstract</jats:title><jats:sec> <jats:title>Purpose</jats:title> <jats:p>The present study explores the dynamics of cell death in Hirschsprung’s disease (HSCR) and control (CO) groups under inflammatory stress conditions.</jats:p> </jats:sec><jats:sec> <jats:title>Methods</jats:title> <jats:p>Using flow cytometry, we analyzed intestinal colonic organoid cultures derived from the ganglionic segment of the HSCR and CO groups. Our analysis focused on the quantification of RIPK1-independent and RIPK1-dependent apoptosis, as well as necroptosis in both viable and non-viable cells under acute and chronic inflammatory stress.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>Our findings indicate that HSCR cells are particularly vulnerable to inflammation during acute proinflammatory stress, as evidenced by an increase in dead cells (Zombie +). Under chronic conditions, adaptive changes are observed in both HSCR and CO groups, indicating survival mechanisms. These adaptations are uniquely altered in HSCR, suggesting an impaired response to chronic inflammation. HSCR cells show significantly decreased RIPK1-dependent apoptosis in acute scenarios compared to chronic ones, unlike the CO group, implying varied responses to different inflammatory stresses. In non-viable cells, considerable changes in RIPK1-dependent apoptosis under chronic conditions in HSCR indicate a heightened inflammatory response compared to CO.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusion</jats:title> <jats:p>This research provides insights into cell death regulation in HSCR under inflammatory stress by using patient-derived organoids, underscoring the complexity of its inflammatory response.</jats:p> </jats:sec>
1000 Sacherschließung
lokal Female [MeSH]
lokal Organoids [MeSH]
lokal RIP3–caspase-3 assay
lokal Humans [MeSH]
lokal Cell Death/physiology [MeSH]
lokal Inflammation [MeSH]
lokal Apoptosis/physiology [MeSH]
lokal Apoptosis
lokal Necroptosis/physiology [MeSH]
lokal Organoids
lokal Flow Cytometry/methods [MeSH]
lokal Colon/pathology [MeSH]
lokal Original Article
lokal Infant [MeSH]
lokal Male [MeSH]
lokal RIK1
lokal Receptor-Interacting Protein Serine-Threonine Kinases/metabolism [MeSH]
lokal Hirschsprung’s disease
lokal Hirschsprung Disease/pathology [MeSH]
lokal Necroptosis
lokal Hirschsprung Disease/metabolism [MeSH]
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/TGksIFpob25nd2Vu|https://frl.publisso.de/adhoc/uri/SGFnZW5zLCBKb2hhbm5h|https://frl.publisso.de/adhoc/uri/UGhpbGlwcGksIENsYXJh|https://frl.publisso.de/adhoc/uri/U2NobWlkdCwgSGFucyBDaHJpc3RpYW4=|https://frl.publisso.de/adhoc/uri/Um9od8OkZGVyLCBMdWNpZQ==|https://frl.publisso.de/adhoc/uri/U2NodXBwZXJ0LCBQYXVsaW5l|https://frl.publisso.de/adhoc/uri/UGFnZXJvbHMgUmFsdXksIExhaWE=|https://frl.publisso.de/adhoc/uri/VHJvY2hpbWl1aywgTWFnZGFsZW5h|https://frl.publisso.de/adhoc/uri/UmVpbnNoYWdlbiwgS29ucmFk|https://frl.publisso.de/adhoc/uri/VG9tdXNjaGF0LCBDaHJpc3RpYW4=
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1000 Label
1000 Förderer
  1. Universitätsklinikum Hamburg-Eppendorf (UKE) |
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1000 Dateien
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    1000 Förderer Universitätsklinikum Hamburg-Eppendorf (UKE) |
    1000 Förderprogramm -
    1000 Fördernummer -
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1000 Erstellt am 2025-07-07T04:51:41.600+0200
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1000 Objekt bearb. Thu Jul 31 08:49:28 CEST 2025
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